Cases reported "Anaphylaxis"

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1/19. Acute anaphylaxis following midline catheterisation in a patient with cystic fibrosis.

    A 16 year old male with cystic fibrosis experienced an acute life threatening anaphylactic reaction following the insertion of an Ohmeda Hydrocath(TM) midline peripheral venous catheter. The catheter was immediately withdrawn and treatment with intravenous adrenaline, hydrocortisone, chlorpheniramine, and colloid over a 24 hour period resulted in a gradual resolution of symptoms.
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2/19. anaphylaxis to chlorhexidine. Case report. Implication of immunoglobulin e antibodies and identification of an allergenic determinant.

    BACKGROUND: There are many reports of allergic reactions, including anaphylaxis, following exposure to chlorhexidine. Reactions may occur via contact with the skin and mucous membranes or from catheters treated with the antibacterial agent. Apart from implicating chlorguanide in immunoglobulin (Ig) E antibody-binding studies on serum from an anaphylactic patient, little work has been done on the molecular basis of recognition of the agent in sensitive subjects. OBJECTIVES: The molecular basis of IgE-binding to chlorhexidine was closely examined with the view of defining its fine structural recognition features by antibodies from a subject who experienced anaphylaxis following contact with the antiseptic. methods: Tryptase determinations, different drug-solid phases, immunoassays and quantitative hapten inhibition studies with chlorhexidine and selected structural analogues were employed together with serum from the anaphylactic patient. Results were analysed to define the complete drug allergenic determinant and to identify the important structural features complementary to the IgE antibody combining sites. RESULTS: The subject's serum tryptase levels sampled after the reaction were elevated and employment of a chlorhexidine-EA sepharose solid phase showed the presence of serum IgE antibodies to the drug. Lack of inhibition by 4-chlorophenol and other selected substituted phenyl compounds showed that the terminal groups at each end of the chlorhexidine molecule, alone, did not account for antibody recognition of the antibacterial agent. Although chlorguanide and alexidine, the structures of which each comprise part of the chlorhexidine molecule, showed significant inhibition of the binding of IgE antibodies to chlorhexidine, neither compound was as potent an inhibitor as chlorhexidine itself. Two molecules of chlorguanide make up the symmetrical molecule of chlorhexidine while the interior structure of alexidine (that is excluding the terminal 2-ethylhexyl groups) is identical to part of the chlorhexidine molecule. CONCLUSIONS: Taken together, for this patient, these results lead to the conclusion that the whole chlorhexidine molecule is complementary to the IgE antibody combining sites and that the 4-chlorophenol, biguanide and hexamethylene structures together comprise the allergenic determinant. Hence, like one of the trimethoprim determinants identified, but unlike most drug allergenic determinants identified so far, the chlorhexidine allergenic determinant identified here encompasses the entire molecule.
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3/19. vancomycin anaphylaxis and successful desensitization in a patient with end stage renal disease on hemodialysis by maintaining steady antibiotic levels.

    BACKGROUND: vancomycin anaphylaxis is a major management problem in patients with methicillin-resistant staphylococcus aureus (MRSA) sepsis. Lerner et al in 1984 have described a protocol for desensitization to vancomycin; however, antibiotic blood levels have never been used as a guide in this process. CASE REPORT: A 46-year-old female with ESRD on hemodialysis who developed a dialysis-catheter related MRSA sepsis was found to have anaphylaxis to vancomycin. She underwent successful desensitization to vancomycin using Lerner's protocol. Periodic antibiotic blood levels were used to guide the amount and frequency of vancomycin infusion to successfully maintain desensitization thereafter. DISCUSSION: Lerner described loss of desensitization to vancomycin when antibiotic infusion was stopped after 18 hours followed by successful desensitization to the same drug via the same protocol. This observation points out that desensitization to vancomycin appears to be dependent on some minimal drug level. In our case report, we have for the first time used the concept of blood levels to maintain successful desensitization to an antibiotic. CONCLUSION: We hypothesize that desensitization to vancomycin can be induced and maintained by keeping a minimum antibiotic blood level. Further studies are needed to quantify this.
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4/19. Two episodes of life-threatening anaphylaxis in the same patient to a chlorhexidine-sulphadiazine-coated central venous catheter.

    chlorhexidine allergy has been described in the literature, mainly in Japanese individuals. Most reactions have been limited to the skin, mild in severity and a result of chlorhexidine containing solutions such as 'Savlon' (Novartis Consumer health, Horesham, UK). We describe what we believe is the first reported case of anaphylaxis in a European patient to a chlorhexidine- sulphadiazine-coated central venous catheter.
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5/19. methylene blue: an effective treatment for contrast medium-induced anaphylaxis.

    BACKGROUND: The purpose of this paper is to propose methylene blue as a lifesaving alternative drug for the treatment of contrast-induced anaphylaxis. CASE REPORT: In a cardiovascular catheterization laboratory invasive hemodynamic monitoring was used to document the lifesaving effect of IV bolus injections of 1.5-2 mg/Kg methylene blue solution to treat three patients for anaphylactic shock following radiocontrast injection during coronary angiography. methylene blue administration was followed by prompt circulatory improvement, leading to hemodynamic stabilization and relief of other anaphylactic symptoms in each case. There were no deaths. CONCLUSIONS: Our findings suggest that methylene blue can be lifesaving in anaphylactic shock, notwithstanding some transitory side effects, such as cardiac rhythm disturbances and chest pain, both of which possibly originate from sudden myocardial perfusion deficits.
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6/19. myocardial ischemia due to severe amoxicillin allergy.

    A patient suffered a myocardial injury as a manifestation of anaphylactic reaction to amoxicillin-clavulanic acid administration. A cardiologic study (ergometry and catheterization) showed no obstructive coronary disease and prick test to amoxicillin was positive. anaphylaxis may cause myocardial injury and the mechanism is likely to be vasospasm induced by mast cells and basophil mediators.
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7/19. Refractory anaphylactic shock associated with ketoconazole treatment.

    OBJECTIVE: To report a rare but severe reaction of refractory anaphylactic shock with ketoconazole treatment-associated hypotensive episodes in an elderly patient. CASE SUMMARY: A 72-year-old woman received antifungal therapy for her almost completely occluded cornea infected with candida albicans. She was initially prescribed oral ketoconazole 200 mg twice daily. She developed hypotension over the first 2 days of therapy (BP 136/82 mm Hg at baseline; 90/50 mm Hg on day 2). Severe hypotension (BP 90/49 mm Hg) unresponsive to fluid therapy or high-dose dopamine developed on day 4 of therapy. An invasive Swan-Ganz catheterization study showed a very low level of peripheral vascular resistance with high cardiac output index without clinical signs of infection. When laboratory tests showed a high level of plasma tryptase, anaphylactic redistribution shock was diagnosed. Her vital signs became more stable after treatment with hydrocortisone and epinephrine infusion. She was discharged in good condition after 24 hours of observation. DISCUSSION: As of December 2004, refractory anaphylactic shock resulting from ketoconazole use had not been reported. The events of hypotension were strongly associated with the intake of ketoconazole. The hemodynamic results obtained with Swan-Ganz catheterization were compatible with anaphylactic shock. The Naranjo probability scale showed a probable association of the adverse event with ketoconazole. CONCLUSIONS: ketoconazole may cause severe anaphylactic shock even when taken orally. Invasive catheterization and elevated tryptase levels can provide important information in the management of anaphylactic shock.
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8/19. anaphylaxis to an urethral lubricant: chlorhexidine as the "hidden" allergen.

    We report on a severe allergic reaction during urethral catheterisation, initially erroneously attributed to natural rubber latex (NRL). However, the negative investigations for latex, the uneventful further applications of NRL, the positive skin test and basophil activation test for chlorhexidine strongly support diagnosis of chlorhexidine anaphylaxis. This case illustrates that it is not widely appreciated that "innocent" products such as urethral lubricants may elicit serious life-threatening reactions. Careful inspection of the medical records is once again re-emphasised to be mandatory in order to avert subsequent anaphylaxis.
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9/19. An unexpected cause of an acute hypersensitivity reaction during recovery from anaesthesia.

    Acute hypersensitivity reactions to chlorhexidine in the operating room are probably more likely to occur during the early phases of anaesthesia because chlorhexidine is often used for cleaning the surgical field or during placement of indwelling catheters. We report a case of an acute hypersensitivity reaction that occurred in the post anaesthetic care unit. Subsequent skin testing suggested sensitivity to chlorhexidine, which had been applied over the vaginal mucosa at the end of surgery. Relevant issues in the investigation of acute hypersensitivity reactions in the post anaesthetic period are discussed.
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10/19. A case of hydrocortisone desensitization in a patient with radiocontrast-induced anaphylactoid reaction and corticosteroid allergy.

    Allergic reactions and systemic desensitization to corticosteroids have been documented rarely in English language literature. These reactions appear more often when the agent is applied topically and may lead to dangerous complications in patients if administered i.v. Therefore, the safety and efficacy of using an i.v. corticosteroid for desensitization in a patient who has a history of allergy to corticosteroid must be weighed carefully, especially when the aim of its use is to prevent an allergic reaction from a second drug. We report a case of successful systemic hydrocortisone desensitization in a patient with radiocontrast-induced anaphylactoid reaction and corticosteroid allergy. Sensitization to corticosteroids was determined through skin testing. The patient was desensitized to hydrocortisone and premedicated with hydrocortisone and diphenhydramine and subsequently underwent cardiac catheterization with radiocontrast without adverse reaction.
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